than in the normal group. However, chronic treatment with curcumin prevented this decrease in GPx activity in the
diabetic group Table 1.
3.5 Effect of curcumin on extracellular matrix
protein expression Increases in the expressions of fibrotic factors, such as TGF-
b
1
, CTGF and osteopontin, and extracellular matrix proteins, such as type IV collagen and fibronectin, are
believed to be partly responsible for the glomerular enlar- gements and fibrosis [25]. Western blotting analysis
demonstrated significant increases of TGF-b
1
and CTGF expression in the diabetic group compared with those in the
normal group, which were significantly attenuated by treatment with curcumin Fig. 3A, C, D. Moreover, protein
expression of osteopontin was also significantly increased in the diabetic group compared with that in the normal
group, which was significantly reduced by curcumin treat- ment Fig. 3A and E. To further evaluate the effect of
curcumin treatment in the STZ-induced DN model, the expressions of type IV collagen and fibronectin were exam-
ined by immunohistochemical staining. The immunor- eactivity of type IV collagen Fig. 4D and fibronectin
Fig. 4E in kidney tissue was increased in the diabetic group compared with that in the normal group. Curcumin
treatment decreased the accumulation of type IV collagen and fibronectin induced by STZ. Semi-quantitative analysis
revealed a significant inhibitory effect of curcumin treat- ment on kidney tissue accumulation of type IV collagen and
fibronectin induced by STZ compared with that of vehicle Fig. 4D1 and E1.
3.6 Effect of curcumin treatment on pro-angiogenic
VEGF and VEGF-RII flk-1 We next examined the expression of pro-angiogenic factor
VEGF and corresponding receptors flk-1 by Western blot analysis and immunohistochemistry, respectively. The
levels of VEGF Fig. 3A and B and flk-1 Fig. 4F, 4F1 were significantly increased in the diabetic group, which were
significantly suppressed by treatment with curcumin.
3.7 p300 level assessed by RT-PCR
Rats with DN had upregulated expression of p300 mRNA in comparison with group N, and the treatment with curcumin
significantly reversed the renal mRNA levels of p300 in rats with DN Fig. 2C.
3.8 Effect of curcumin against renal histological
